Abstract
Biochemical mechanisms that control the levels and function of key tumor suppressor proteins are of great interest as their alterations can lead to oncogenic transformation. Here, we identify the human orthologue of Drosophila melanogaster ecdysoneless (hEcd) as a novel p53-interacting protein. Over-expression of hEcd increases the levels of p53 and enhances p53 target gene transcription whereas hEcd knockdown has the opposite effects on p53 levels and target gene expression. Furthermore, hEcd interacts with murine double minute-2 and stabilizes p53 by inhibiting murine double minute-2-mediated degradation of p53. Thus, hEcd protein represents a novel regulator of p53 stability and function. Our studies also represent the first demonstration of a biochemical function for hEcd protein and raise the possibility that altered hEcd levels and/or function may contribute to oncogenesis.
Original language | English (US) |
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Pages (from-to) | 7167-7175 |
Number of pages | 9 |
Journal | Cancer Research |
Volume | 66 |
Issue number | 14 |
DOIs | |
State | Published - Jul 15 2006 |
Externally published | Yes |
ASJC Scopus subject areas
- Oncology
- Cancer Research